https://scholars.lib.ntu.edu.tw/handle/123456789/188404
標題: | 心包膜腔內注入 Neuropeptide Y以誘發缺氧心肌之血管新生–豬之動物實驗模式 | 作者: | 廖朝崧 | 關鍵字: | 血管新生;側枝循環;心包膜穿刺;冠動脈病;心肌缺氧;angiogenesis;collateral circulation;pericardial drug administration;coronary artery disease;myocardial ischemia | 公開日期: | 2005 | 出版社: | 臺北市:國立臺灣大學醫學院內科 | 摘要: | 有些冠狀動脈心臟病病人由於嚴重且廣泛之冠狀動脈阻塞,導致嚴重心肌缺 氧,一般採行之血管再通術完全無法施行。目前發現有一些血管新生促進物資可 加強側枝循環之形成,但至目前為止僅有FGF 及VEGF 在臨床上使用。 Neuropeptide Y (NPY)已經證實為一種強力之血管新生因子。心包膜腔對心肌 而言應是一個很適當的給藥途徑,可以長時間發揮治療效果。本實驗擬將 Neuropeptide Y 注入已誘發心肌梗塞的豬之心包膜腔內,以觀察其對缺氧之心肌誘 發血管新生的功效。 我們進行三組實驗,即NPY 組,對照組及心包沾粘組。首先在實驗豬以冠狀 動脈堵塞法引發急性心肌梗塞,大多堵塞左前下行冠狀動脈。經1-3 星期後,將藥 物(NPY 或minocyclin)或僅給生理食鹽水注入心包膜腔。NPY 組共有10 隻豬, 每隻打入NPY 0.5 mg/5 西西無菌水。對照組有10 隻豬,只打入normal saline 。心 包沾粘組共有9 隻豬,在AMI 後1-2 星期在心包膜腔打入minocyclin 。在AMI 後 4-7 星期,將實驗豬犧牲,取其心臟作觀察,測量,並作顯微鏡觀察。 在本實驗中我們發現,在心包膜腔打入NPY 並不能在心肌梗塞部位隣近之心 肌內誘發血管增生,但接受NPY 之實驗豬其心臟重量較低,此為一有利之變化。 我們也發現,左心室壁厚度及心肌梗塞大小並不因打入NPY 或minocyclin 而有所 改變。但出乎意料的,我們發現,心包膜腔注入minocyclin 可誘發血管之增生。此 一發現值得更進一步之研究。 There are patients with coronary artery disease who suffered from severe and diffuse narrowing or occlusion of their coronary arteries, in whom the conventional revascularization procedures can not be applied. One potential strategy for these patients is creation of new blood vessel channels in the region of ischemia, (therapeutic angiogenesis). A number of potential angiogenic agents have been identified to enhance the process of collateral development, but, to date, only two growth factors, fibroblastic growth factor (FGF) and vascular endothelial growth factor (VEGF), have been clinically used in patients with refractory ischemia. Neuropeptide Y (NPY) has been proved as one of the potent growth factors for angiogenesis. The pericardial space may potentially serve as a drug delivery reservoir which may render persistent effects of the administered therapeutic agents to the heart. In this experiment, we tested the effects of NPY administered through pericardial chamber on the angiogenesis of ischemic myocardium in a porcine myocardial infarction model. We performed experiments on 3 groups of pigs, the neuropeptide Y (NPY) group, the control group, and the adhesion group. Acute myocardial infarction (AMI) was first induced in all experimental pigs by occlusion of a coronary artery, left anterior descending artery in most pigs. After 1-3 weeks, either drug administration (NPY or minocyclin) or non-specific drug (saline) administration (control group) was performed. The NPY group consisted of 10 pigs, in them NPY 0.5 mg in 5 ml sterile water was administrated through a catheter into the pericardium. In the control group, 10 pigs, after induction of AMI, only saline intrapericardial administration was applied. In the adhesion group, 9 pigs, minocyclin was administrated into pericardial sac 1-2 weeks after AMI to induce pericardial adhesion. Pigs were sacrificed 4-7 weeks after induction of AMI and the hearts were measured grossly and examined microscopically. In this study we found that administration of NPY did not induce new vessel production in the myocardium near the infarction area. Yet, the administration of NPY seemed to result in reduced heart weight, a beneficial effect. We also found that the wall thickness of LV wall as well as the infarction size was not affected by the administration of either NPY or minicyclin. Incidentally, we found that intrapericardial administration of minicyclin could induce active new vessel growth in the myocardium near the infarction area. This finding may be worthy of further studies. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/23709 | 其他識別: | 932314B002222 | Rights: | 國立臺灣大學醫學院內科 |
顯示於: | 醫學系 |
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932314B002222.pdf | 1.22 MB | Adobe PDF | 檢視/開啟 |
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